As illustrated in FIG. 1, the human heart (10) has four chambers which include two upper chambers denoted as atria (12, 16) and two lower chambers denoted as ventricles (14, 18). A septum (20) divides the heart and separates the left atrium (12) and left ventricle (14) from the right atrium (16) and right ventricle (18). The heart further contains four valves (22, 24, 26 and 28). The valves function to maintain the pressure and unidirectional flow of the blood through the body and to prevent the blood from leaking back into a chamber from which it has been pumped.
Two valves separate the atria (12, 16) from the ventricles (14, 18), denoted as atrioventricular valves. The left atrioventricular valve, the mitral valve (22), controls the passage of oxygenated blood from the left atrium (12) to the left ventricle (14). A second valve, the aortic valve (24), separates the left ventricle (14) from the aortic artery (aorta) (30), which delivers oxygenated blood via the circulation to the entire body. The aortic and mitral valves are part of the “left” heart, which controls the flow of oxygen-rich blood from the lungs to the body. The right atrioventricular valve, the tricuspid valve (26), controls passage of deoxygenated blood into the right ventricle (18). A fourth valve, the pulmonary valve (28), separates the right ventricle (18) from pulmonary artery (32). The right ventricle (18) pumps deoxygenated blood through the pulmonary artery (32) to the lungs wherein the blood is oxygenated and then delivered to the left atrium (12) via the pulmonary vein. Accordingly, the tricuspid (26) and pulmonic (28) valves are part of the “right” heart, which control the flow of oxygen-depleted blood from the body to the lungs.
Both the left and right ventricles (14 and 18, respectively) constitute “pumping” chambers. The aortic (24) and pulmonic (28) valves lie between a pumping chamber (ventricle) and a major artery and control the flow of blood out of the ventricles and into the circulation. The aortic and pulmonary valves have three cusps, or leaflets, that open and close and thereby function to prevent blood from leaking back into the ventricles after being ejected into the lungs or aorta for circulation.
Both the left and right atria (14 and 16, respectively) are “receiving” chambers. The mitral (22) and tricuspid (26) valves, therefore, lie between a receiving chamber (atrium) and a ventricle so as to control the flow of blood from the atria to the ventricles and prevent blood from leaking back into the atrium during ejection into the ventricle. Both the mitral (22) and tricuspid (26) valves include two or more cusps, or leaflets (not shown), that are encircled by a variably dense fibrous ring of tissues known as the annulus (not shown). The valves are anchored to the walls of the ventricles by chordae tendineae (chordae) (42). The chordae tendineae (42) are cord-like tendons that connect the papillary muscles (44) to the leaflets (not shown) of the mitral (22) and the tricuspid (26) valves of the heart (10). The papillary muscles (44) are located at the base of the chordae (42) and are within the walls of the ventricles. They serve to limit the movements of the mitral (22) and tricuspid (26) valves and prevent them from being reverted. The papillary muscles do not open or close the valves of the heart, which close passively in response to pressure gradients; rather, the papillary muscles brace the valves against the high pressure needed to circulate the blood throughout the body. Together, the papillary muscles (44) and the chordae tendineae (42) are known as the subvalvular apparatus. The function of the subvalvular apparatus is to keep the valves from prolapsing into the atria when they close.
As illustrated with reference to FIG. 2, the mitral valve (100) includes two leaflets, the anterior leaflet (102) and the posterior leaflet (104), and a diaphanous incomplete ring around the valve, the annulus (110). The mitral valve contains two papillary muscles (not shown), the anteromedial and the posterolateral papillary muscles, which attach the leaflets to the walls of the left ventricle via the chordae tendineae (not shown). The tricuspid valve typically is made up of three leaflets and three papillary muscles. However, the number of leaflets can range between two and four. The three leaflets of the tricuspid valve are referred to as the anterior, posterior, and septal leaflets. Although both the aortic and pulmonary valves each have three leaflets (or cusps) they do not have chordae tendineae.
Various disease processes can impair the proper functioning of one or more of the valves of the heart. These disease processes include degenerative processes (e.g., Barlow's Disease, fibroelastic deficiency), inflammatory processes (e.g., Rheumatic Heart Disease) and infectious processes (e.g., endocarditis). Additionally, damage to the ventricle from prior heart attacks (i.e., myocardial infarction secondary to coronary artery disease) or other heart diseases (e.g., cardiomyopathy) can distort the valve's geometry causing it to dysfunction. However, the vast majority of patients undergoing valve surgery, such as mitral valve surgery, suffer from a degenerative disease that causes a malfunction in a leaflet of the valve which results in prolapse and regurgitation.
Generally, there are two different ways that a heart valve may malfunction. One possible malfunction, valve stenosis, occurs when a valve does not open completely and thereby causes an obstruction of blood flow. Typically, stenosis results from buildup of calcified material on the leaflets of the valves causing them to thicken and thereby impairing their ability to fully open and permit adequate forward blood flow.
Another possible malfunction, valve regurgitation occurs when the leaflets of the valve do not close completely thereby causing blood to leak back into the prior chamber. There are three mechanisms by which a valve becomes regurgitant or incompetent; they include Carpentier's type I, type II and type III malfunctions. A Carpentier type I malfunction involves the dilation of the annulus such that normally functioning leaflets are distracted from each other and fail to form a tight seal (i.e., do not coapt properly). Included in a type I mechanism malfunction are perforations of the valve leaflets, as in endocarditis. A Carpentier's type II malfunction involves prolapse of one or both leaflets above the plane of coaptation. This is the most common cause of mitral regurgitation, and is often caused by the stretching or rupturing of chordae tendinae normally connected to the leaflet. A Carpentier's type III malfunction involves restriction of the motion of one or more leaflets such that the leaflets are abnormally constrained below the level of the plane of the annulus. Leaflet restriction can be caused by rheumatic disease (IIIa) or dilation of the ventricle (IIIb).
FIG. 3 illustrates a prolapsed mitral valve (200). As can be seen with reference to FIG. 3, prolapse occurs when a leaflet (202 or 204) of the mitral valve (200) is displaced into the left atrium during systole. Because one or more of the leaflets malfunction the valve does not close properly, and, therefore, the leaflets fail to coapt. This failure to coapt causes a gap between the leaflets (202 and 204) that allows blood to flow back into the left atrium, during systole, while it is being ejected into the left ventricle. As set forth above, there are several different ways a leaflet may malfunction, which can thereby lead to regurgitation.
Although stenosis or regurgitation can affect any valve, stenosis is predominantly found to affect either the aortic and pulmonary valves, whereas regurgitation predominately affects either the mitral or tricuspid valve. Both valve stenosis and valve regurgitation increase the workload on the heart and may lead to very serious conditions if left un-treated; such as endocarditis, congestive heart failure, permanent heart damage, cardiac arrest and ultimately death. Since the left heart is primarily responsible for circulating the flow of blood throughout the body, malfunction of the mitral or aortic valves is particularly problematic and often life threatening. Accordingly, because of the substantially higher pressures on the left side of the heart, left-sided valve dysfunction is much more problematic.
Malfunctioning valves may either be repaired or replaced. Repair typically involves the preservation and correction of the patient's own valve. Replacement typically involves replacing the patient's malfunctioning valve with a biological or mechanical substitute. Typically, the aortic and the pulmonary valves are more prone to stenosis. Because stenotic damage sustained by the leaflets is irreversible, the most conventional treatment for stenotic aortic and pulmonic valves is the removal and replacement of the diseased valve. The mitral and the tricuspid valves, on the other hand, are more prone to deformation. Deformation of the leaflets, as described above, prevents the valves from closing properly and allows for regurgitation or back flow from the ventricle into the atrium, which results in valvular insufficiency. Deformations in the structure or shape of the mitral or tricuspid valve are often repairable.
Valve repair is clearly preferable to valve replacement. Bioprosthetic valves have limited durability. Secondly, prosthetic valves rarely function as well as the patient's own valves. Additionally, there is an increased rate of survival and a decreased mortality rate and incidence of endocarditis for repair procedures. Further, because of the risk of thromboembolism, mechanical valves often require further maintenance, such as the lifelong treatment with blood thinners and anticoagulants. Therefore, an improper functioning mitral or tricuspid valve is ideally repaired, rather than replaced. However, because of the complex and technical demands of the repair procedures, the overall repair rate in the United States is only around 50%.
Conventional techniques for repairing a cardiac valve are labor-intensive, technically challenging, and require a great deal of hand-to-eye coordination. They are, therefore, very challenging to perform, and require a great deal of experience and extremely good judgment. For instance, the procedures for repairing regurgitating leaflets may require resection of the prolapsed segment and insertion of an annuplasty ring so as to reform the annulus of the valve. Additionally, leaflet sparing procedures for correcting regurgitation are just as labor-intensive and technically challenging, if not requiring an even greater level of hand-to-eye coordination. These procedures involve the implantation of sutures (e.g., ePTFE or GORE-TEX™ sutures) so as to form artificial chordae in the valve. In these procedures, rather than performing a resection of the leaflets and/or implanting an annuplasty ring into the patient's valve, the prolapsed segment of the leaflet is re-suspended using artificial chord sutures. Oftentimes, leaflet resection, annuplasty and neo-cord implantation procedures are performed in conjunction with one another.
Regardless of whether a replacement or repair procedure is being performed, conventional approaches for replacing or repairing cardiac valves are typically invasive open-heart surgical procedures, such as sternotomy or thoracotomy, that require opening up of the thoracic cavity so as to gain access to the heart. Once the chest has been opened, the heart is bypassed and stopped. Cardiopulmonary bypass is typically established by inserting cannulae into the superior and inferior vena cavae (for venous drainage) and the ascending aorta (for arterial perfusion), and connecting the cannulae to a heart-lung machine, which functions to oxygenate the venous blood and pump it into the arterial circulation, thereby bypassing the heart. Once cardiopulmonary bypass has been achieved, cardiac standstill is established by clamping the aorta and delivering a “cardioplegia” solution into the aortic root and then into the coronary circulation, which stops the heart from beating. Once cardiac standstill has been achieved, the surgical procedure may be performed. These procedures, however, adversely affect almost all of the organ systems of the body and may lead to complications, such as strokes, myocardial “stunning” or damage, respiratory failure, kidney failure, bleeding, generalized inflammation, and death. The risk of these complications is directly related to the amount of time the heart is stopped (“cross-clamp time”) and the amount of time the subject is on the heart-lung machine (“pump time”).
Furthermore, the conventional methods currently being practiced for the implantation of the artificial chordae are particularly problematic. Because the conventional approach requires the heart to be stopped (e.g., via atriotomy) it is difficult to accurately determine, assess and secure the appropriate chordal length. Since the valve will not function properly if the length of the artificial chordae is too long or too short, the very problem sought to be eradicated by the chordal replacement procedure may, in fact, be exacerbated. Using conventional techniques, it is very difficult to ensure that the chordae are of the correct length and are appropriately spaced inside the ventricle to produce a competent valve.
Accordingly, there is a continuing need for new procedures for performing cardiac valve repairs, such as mitral and tricuspid valve repairs, that are less invasive, do not require cardiac arrest, and are less labor-intensive and technically challenging. Chordal replacement procedures that ensure the appropriate chordal length and spacing so as to produce a competent valve are of particular interest. The methods presented herein meet these needs.